From the authors:
J.C. Grignola points out that the product of pulmonary vascular resistance by pulmonary vascular compliance, or time constant (RC time) of the pulmonary circulation is not truly constant, and that this impacts on the pulsatile component (Wosc) of right ventricular hydraulic load (Wtot).
He is right. But the question is, by how much? In the experimental study by Pagnamenta et al. [1], pulmonary hypertension induced by ensnarement of the pulmonary arteries, to mimic purely proximal chronic thromboembolic pulmonary hypertension (CTEPH), was associated with a decrease in RC time from 0.5 s to 0.3 s, while microembolism to mimic purely distal obstruction, like in pulmonary arterial hypertension (PAH), was associated with an increase in RC time from 0.5 s to 0.8 s. Associated changes in Wosc/Wtot went from 25% to 29% and 16%, respectively. These would be the extreme possible deviations of a fixed Wosc/Wtot of 23% calculated for all types and severities of pulmonary hypertension by Saouti et al. [2] on the basis of recovered constant RC times. In other words, Wtot, as an estimation of right ventricular afterload, is not always equal to 1.3×steady-flow W (calculated as the product of mean pulmonary artery pressure and stroke volume) proposed by Saouti et al. [2], but in the range 1.2–1.4. This is not much. Furthermore, as also underscored by J.C. Grignola [1], vascular obstruction in clinical pulmonary hypertension tends to be inhomogeneous and spread over the entire vascular tree, especially in CTEPH, so that the variations of the estimate of Wtot would be markedly smaller, probably reduced to somewhere between 1.25 and 1.35×steady-flow W. This corresponds to trivial variations in afterload. Unsurprisingly, as illustrated in figure 1a of J.C. Grignola’s correspondence, the reported range of RC times has a minimal effect on the proportionality of systolic, mean and diastolic pulmonary artery pressures. Conversely, the near-constant RC time in pulmonary hypertension is still in marked contrast with the extensive variability of the systemic RC time [3].
The discovery of “laws of nature” in medical research clarifies understanding and is essential for bedside translation of bench research. The repeated observations by Lankhaar et al. [4] that RC time is constant in the pulmonary circulation has helped considerably in the assessment of right ventricular afterload in pulmonary hypertension. But scientific truth has to be constantly rechallenged, and uncovering exceptions leads to developments of new paradigms and innovation. J.C. Grignola is to be commended for pointing out that the RC time is shortened in left heart failure with increased pulmonary venous pressure, which makes the pulmonary circulation less compliant at any given level of resistance [3], and in operable CTEPH because of increased wave reflection and proximal arterial stiffness [5]. However, the deviations are small, so that the general rule of the constancy of the RC time remains a reasonable approximation in all circumstances.
Thus, while we agree with J.C. Grignola’s pertinent remarks, we humbly feel allowed to maintain our statement that the RC time of the pulmonary circulation is approximately the same in CTEPH and PAH [6], indicating surprisingly little impact of proximal obstruction-related increased wave reflection or stiffness on right ventricular afterload.
Footnotes
Conflict of interest: Disclosures can be found alongside the online version of this article at www.erj.ersjournals.com
- Received October 6, 2013.
- Accepted October 8, 2013.
- ©ERS 2014